PaCO2 and the Post-Arrest Patient
It is well known that the early aggressive utilization of IV nitrates and non-invasive positive pressure ventilation (NIV) in patients presenting with acute pulmonary edema will decrease the number of patients requiring endotracheal intubation and mechanical ventilation.
Often our tepid dosing of nitroglycerine is to blame for treatment failure. Multiple studies have demonstrated the advantages of bolus dose nitroglycerine in the early management of patients with acute pulmonary edema. In these cohorts, patients bolused with impressively high doses of IV nitrates every 5 minutes, are intuabted less frequently than patients who received a standard infusion (1,2). No concerning drops in blood pressure in the patients who received bolus doses of nitrates were observed. Using the standard 200 micrograms/ml nitroglycerine concentration, blood pressure can be rapidly titrated to effect.
The Neurocritical Care Society and Society of Critical Care Medicine just came out with new Guidelines for Reversal of Antithrombotics in Intracranial Hemorrhage (ICH) [1]
--PCC is now recommended over FFP in reversal of vitamin K antagonists (VKA) with elevated INR. Either should be co-administered with 10mg IV vitamin K. (Strong recommendation, moderate quality evidence)
TAKE AWAY: PCC should be probably be given over FFP in VKA-ICH when available
Mechanical Ventilation in the Obese Patient
The prognosis of patients who experienced OHCA, who have not achieved ROSC by the time they present to the Emergency Department, is dismal. As such, it behooves us as Emergency Physicians to identify the few patients with a potentially survivable event. Drennan et al examined the ROC data base and identified the cohort of patients who had not achieved ROSC and were transported to the hospital. The overall survival in this cohort was 2.0%. Factors that predicted survival were initial shockable rhythm and arrest witnessed by the EMS providers. Patients arriving to the ED without ROSC, that had neither of those prognostic factors had a survival rate of 0.7%.
--In this study, PE was diagnosed in ~17% of patients hospitalized for syncope (though this represents only ~4%% of patients presenting to the ED with syncope).
--Patients with PE were more likely to have tachypnea, tachycardia, relative hypotension, signs of DVT, and active cancer -- take a good history and do a good physical exam!
--Consider risk stratifying (Wells/Geneva) and/or performing a D-dimer (i.e "rule out" PE) on your syncope patients, particularly when no alternative diagnosis is apparent.
What Matters in Cardiac Arrest?
It is well documented that when left to our own respiratory devices we will consistently over-ventilate patients presenting in cardiac arrest (1). A simple and effective method of preventing these overzealous tendencies is the utilization of a ventilator in place of a BVM. The ventilator is not typically used during cardiac arrest resuscitation because the high peak-pressures generated when chest compressions are being performed cause the ventilator to terminate the breath prior to the delivery of the intended tidal volume. This can easily be overcome by turning the peak-pressure alarm to its maximum setting. A number of studies have demonstrated the feasibility of this technique, most recently a cohort in published in Resuscitation by Chalkias et al (2). The 2010 European Resuscitation Council guidelines recommend a volume control mode targeting tidal volumes of 6-7 mL/kg and a respiratory rate of 10 breaths/minute (3).
It's Election Day in the US, so here are some interesting facts about Presidential causes of death:
George Washington likely died from epiglottitis on 12/14/1799
CLICK BELOW FOR MORE INTERESTING FACTS!
Dynamic LVOT Obstruction
Recently Emergency Physicians have become far more aware of the importance of right ventricular (RV) function in our critically ill patient population. One of the methods that has been proposed to assess RV systolic function with bedside ultrasound (US) is the tricuspid annular plane systolic excursion (TAPSE). This simple bedside measurement utilizes M-mode to quantify the movement of the tricuspid annulus in systole. And while it has demonstrated reasonable accuracy at predicting RV dysfunction, adequate visualization of the lateral tricuspid annulus is not always obtainable in our critically ill patient population (1,2). In these circumstances an alternative measurement obtained in the subcostal window may be a viable option.
Similar to TAPSE, subcostal echocardiographic assessment of tricuspid annular kick (SEATAK) utilizes M-mode to assess the apical movement of the tricuspid annulus during systole. In a recent prospective observational study, Díaz-Gómez et al examined 45 ICU patients, 20 with known RV dysfunction and 25 with normal function. They compared the measurements obtained from TAPSE and SEATAK and found a strong correlation between the two measurement (Spearman’s ρ coefficient of .86, P=.03).
The small sample size and limited evaluation of RV function is far from ideal and more robust data sets are required before we cite SEATAK’s diagnostic accuracy with any confidence, but in the subset of patients where a TAPSE is unobtainable this may serve as an adequate surrogate until a more thorough echographic assessment can be obtained. 
--Massive PE is defined as PE with obstructive shock (hypotension [SBP <90] or end-organ malperfusion)
--Consider venoarterial (VA) ECMO in massive PE for hemodynamic support, particularly prior to intubation
--VA ECMO may prevent intubation/mechanical ventilation, surgical intervention, systemic and local thrombolysis
Oxygen-ICU Trial
The delta gap is a measurement intended to assess for mixed acid-base disorders. A straightforward alternative, the strong ion difference (SID), allows for a quick and simple assessment of any non-gap acidosis or alkalosis that may be present.
The SID is simply the difference between the strong cations (Na+, K+, Mg+, Ca+) and the strong anions (Cl-) present in the serum. The abbreviated SID is the difference between the serum sodium and serum chloride levels (approximately 138-102). Values typically range from 36-40 mg/dl. Values less than 36 denote the presence of some degree of hyperchloremic, non-gap, acidosis. While values greater than 40 demonstrate the presence of hypochloremic, non-gap, alkalosis. And while on rare occasions, variations in albumin or elevated levels of cations other than sodium can lead you astray, the SID is as accurate as a delta gap at identifying mixed acid-based disorders without the added mathematical complexity.
TAKE HOME POINTS:
-- High chloride load is associated with adverse outcomes in large-volume resuscitation (>60mL/kg in 24h), including increased risk of death [1]
-- Avoid supraphysiologic chloride solutions (i.e. normal saline) when resuscitation volumes are likely to exceed 60mL/kg (e.g. sepsis, DKA)
Pitfalls with PLR
--Aggressive BP management (SBP <140) in atraumatic intracerebral hemorrhage (ICH) does NOT signifcantly improve mortality or disability compared with traditional goal (SBP <180) [1]
--However, a lower goal (SBP <140) has been shown to decrease hematoma size and be safe compared to a higher goal (SBP <180) [2]
Ketamine for RSE?
Is it possible to have a patient present in diabetic ketoacidosis (DKA) with both negative serum and urinary ketone levels?
A case report published in American Journal of Emergency Medicine by Jehle et al provides a helpful reminder of this phenomenon (1). The degree of acidosis is directly related to the ratio of the various ketones/ketone metabolites: acetone, acetoacetate and beta-hydroxybutyrate present in the serum. The proportion of each respective substance is determined by the existing redox state in the blood. At any given time, acetoacetate and beta-hydroxybutyrate exist in an equilibrium dependent upon the ratio of NAD+ and NADH(fig.1). These substances freely convert with the assistance of the enzyme beta-
hydroxybutyrate dehydrogenase (2). This conversion requires the donation of a hydrogen atom from NADH. The balance between beta-hydroxybutyrate and acetoacetate, is determined by the ratio of NADH to NAD+. Acetoacetate will freely degrade into acetone through non-enzymatic decarboxylation. Early in DKA, acetoacetate is the most prevalent substance. As the disease progresses and the serum ratio of NADH to NAD+ increases, the proportion of beta-hydroxybutyrate rises, decreasing the quantity of acetoacetate and acetone.
Traditional serum and urinary ketone assays react strongly to acetoacetate but neither reliably react with beta-hydroxybutyrate. Patients in whom the majority of their anion gap is filled by beta-hydroxybutyrate, urinary or serum ketone levels may be negative. In such cases, serum beta-hydroxybutyrate assays would be positive but are not universally available.
It is important to note, with resuscitation and insulin therapy, the ratio of NADH/NAD+ will start to normalize causing an increase in the quantity of acetoacetate. As the patient improves and the anion gap clears, the degree of ketones detected in the serum and urine will paradoxically increase.
Zika Virus-associated GBS
